Resp Week 8 Flashcards

1
Q

describe the epidemiology of SARS-CoV-2 in regards to virus factors

A

virus genome mutates, leading to changes in viral proteins

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2
Q

describe the epidemiology of SARS-CoV-2 in regards to virus transmission

A

zoonotic infection

respiratory transmission

faecal-oral transmission

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3
Q

describe the epidemiology of SARS-CoV-2 in regards to host factors

A

receptors expressed by different hosts, ACE2, contact w animals, air travel and other human behaviours

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4
Q

outline the pathophysiology of SARS-CoV-2

A

infection of endothelial cells

then, spread of virus

then, innate immune response

then, cytokine storm

then, ARDS

then, activation of ACE-2

then, post COVID symptoms

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5
Q

what are the two phases of COVID19 infection

A

rapid viral propagation

uncontrolled inflammatory responses (cytokine storm)

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6
Q

what are 4 stages of the rapid viral propagation phase of COVID19 infection

A

exposure and entry

initial replication

symptom onset

viral shedding

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7
Q

what happens during exposure and entry in rapid viral propagation of COVID19

A

infection begins w exposure to SARS-CoV-2 virus, which then enters body through respiratory tract

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8
Q

what happens during initial replication in rapid viral propagation of COVID19

A

virus rapidly replicates in the upper respiratory tract, and then spreads to the lower respiratory tract where it can infect the lungs

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9
Q

what happens during symptom onset in rapid viral propagation of COVID19

A

many may remain asymptomatic or experience mild to moderate symptoms e.g fever, cough, sore throat, loss of taste/smell

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10
Q

what happens during viral shedding in rapid viral propagation of COVID19

A

infected individuals can shed virus and are contagious during this phase, contributing to spread of disease to others

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11
Q

describe what happens during the uncontrolled inflammatory responses (cytokine storm)

A

virulence often accompanied by programmed cell death

this contributes to clearance of infected cells from body thus preventing further replication of virus

however PCD releases pro-inflammatory cytokines in high quantities leading to what is known as a cytokine storm (e.g PAMPs, DAMPs and cellular cytokines)

the disregulated release of pro inflammatory mediators leads to end organ damage

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12
Q

what are 7 common symptoms associated w COVID 19

A

fever

cough

fatigue

anosmia

sore throat

dyspnea

headache

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13
Q

outline acute respiratory distress syndrome (ARDS)

A

during the second phase of COVID19, body can enter acute respiratory distress whereby its pneumocytes lose the ability to secrete surfactant

this is due to physiological and structural changes in the lung tissue itself, due to acute lung injury at the hands of dysregulated pro inflammatory cytokine release

can lead to tachypnoea, dyspnoea, low blood o2, rattling sounds upon auscultation of lungs

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14
Q

what are 4 prevention methods for COVID 19

A

social distancing

mask wearing

vaccination

hand hygiene

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15
Q

what are 3 pharmacological treatments for management of COVID19

A

analgesics

antivirals

O2 therapy

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16
Q

what are 5 aetiological classifications of pneumonia

A

bacterial - often streptococcus pneumoniae

viral - such as influenza or RSV

aspiration - foreign material, typically gastric contents

atypical - pathogens such as mycoplasma or chlamydia

opportunistic - individuals w weakened immune systems

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17
Q

what are 3 acquisition based classifications of pneumonia

A

community acquired - outside of healthcare settings often caused by common bacteria/viruses

healthcare acquired - during or after hospitalisation/healthcare settings often involving drug-resistant bacteria

ventilator associated - Pt on mechanical ventilation often due to hospital acquired infections

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18
Q

what are 8 symptoms/signs of pneumonia

A

productive cough

dyspnea

pleuritic chest pain

hypoxia

dullness to percussion

decreased breath sounds

bronchial breathing

coarse crackles

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19
Q

outline the pathophysiology of pneumonia

A

underlying agent e.g bacteria, virus etc

then, colonisation of nasopharynx

then, micro-aspiration

then, colonisation of lung parenchyma

then, programmed cell death

then, release of pro-inflammatory cytokines

then, systemic inflammatory response

then, end organ and systemic inflammatory-associated damage

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20
Q

what are 5 complications of pneumonia

A

sepsis

lung abscess

respiratory failure

kidney failure

neurological effects

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21
Q

describe the severity parameters for pneumonia

A

SMART-COP criteria:
systolic BP < 90
multi lobar CXR involvement
albumin <3.5
resp rate >30/min
tachycardia
confusion
O2 sat <90
pH <7.35

5-6 points = high risk of needing IRVS
7+ points = v high risk of needing IRVS

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22
Q

outline the investigative process in diagnosing pneumonia

A

complete blood count - looking for high white cell count and raised inflammatory markers

EUCA - looking for renal fn implications

viral swab - looking for presence of underlying viral contributor

sputum MCS - looking for bacterial contributors

CXR - looking for consolidation and empyema

bronchoscopy

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23
Q

describe the role of bronchoscopy in the investigation of pulmonary infection

A

use of flexible camera and attached suction device to suck out mucous from the lungs

enters via oral or nasal cavity

24
Q

what are 4 management options for pneumonia

A

antibiotics

symptomatic alleviation

supportive management

nutrition assessment

25
outline the pathogenesis of tuberculosis
M.tuberculosis enters the upper airways then, attempted phagocytosis by alveolar macrophages then, M.tuberculosis migrates to lymph nodes and activates B and T cells OR if it survives then it migrates to lung parenchyma then, B and T cells enable macrophages to differentiate into epithelioid cells then, there is fusion of epithelioid cells to form granuloma then, granuloma encases M.tuberculosis preventing its spread and proliferation
26
what are two characteristics of M.tuberculosis that make it trickier to treat
slow growth waxy cell wall
27
what are 8 symptoms/signs of TB
chronic cough haemoptysis chest pain dyspnea loss of appetite night sweats fatigue pallor, wasted appearance and clubbing upon general inspection
28
what are 5 extrapulmonary signs/symptoms of TB
haematuria - due to TB of kidney headache - due to TB meningitis back pain - due to TB of spine hoarseness - due to TB of larynx abdominal discomfort - peritoneal TB
29
what are 4 investigations that can be done in the diagnosis of TB
sputum microscopy sputum culture drug sensitivity CXR
30
what are 6 common complications of TB
pleural effusion haematogenous TB cardiac TB ocular TB hepatic TB GI TB
31
what is the recommended management for bacterial pneumonia
Rx w specific antibiotics (e.g amoxycillin for S.pneumoniae)
32
what is the recommended management for viral pneumonia
Rx w oseltamivir (antiviral) ONLY in cases of individuals w risk factors for poor outcomes of influenza (e.g pregnant) and then cease immediately when influenza is ruled out
33
what is the recommended management for TB in the intensive phase (bactericidal)
Rx for 2 months: isoniazid rifampicin pyrazinamide ethambutol
34
what is the recommended management for TB in the continuation phase (sterilisation)
Rx for 4 months: isoniazid rifampicin
35
what is directly observed therapy (DOT)
describes administration of therapy in a way that is observable by the practitioner enables compliance recommended for individuals w cultural barriers, mental or cognitive pathologies, or those who are at high risk of fatal consequences
36
describe acute vs chronic chest infection
acute = <3 weeks / anything longer = chronic chronic is characterised by stability and interruptions by exacerbations pathogenesis of chronic chest infection is a vicious cycle (it results from the inflammation and creates a cycle towards further infection in the chronically damaged lung)
37
what are 4 risk factors for chronic chest infection
inability to clear secretions reduced respiratory effort decreased cough or gag reflex immunocompromised patients
38
what are 4 symptoms of persistent chest infection
productive cough malaise chest pain fever
39
what are 6 Rx methods for management of persistent chest infection
antibiotics airway clearance vaccination education smoking cessation emergency pack use
40
describe the pathogenesis of bronchiecstasis
impaired drainage/obstruction - impairment of mucus clearance and drainage within airways due to structural abnormalities leading to mucus accumulation and bacterial growth host response - body's immune system mounts prolonged defence, contributing to tissue damage and the perpetuation of the condition transmural inflammation - inflammation that extends through the full thickness of the airway wall, leading to structural changes in the bronchi and bronchioles
41
outline the pathophysiology of bronchiectasis
acquired immunodeficiency, autoimmune, congenital, endobronchial obstruction, or other factors such as inhalation exposure or COPD leads to irreversibly dilated bronchi, chronic bronchial infection and inflammation and easily collapsible airways, resulting in bronchiectasis
42
what are 5 signs/symptoms of bronchiectasis
productive cough dyspnea sleep disturbances changes in appetite systemic infection
43
what are 5 investigative processes that can be done in the diagnosis of bronchiectasis
history/exam sputum culture CXR lung function test CBE
44
what are 5 general management methods for bronchiectasis
physical therapy positive airway pressure antibiotic therapy pulmonary rehab smoking cessation
45
describe the epidemiology of cystic fibrosis
3538 ppl living with CF median age of diagnosis is 20.2 years CF is most common life-limiting disease in australia CF is predominantly inherited by caucasians
46
describe class 1 CF
caused by a mutation that results in the absence of functional CFTR protein, leading to severe disease w minimal to no CFTR activity
47
describe class 2 CF
associated w mutations that result in defective CFTR protein processing and reduced function, causing moderate to severe symptoms
48
describe class 3 CF
involves mutations leading to partially functional CFTR protein, resulting in variable and typically milder disease symptoms
49
describe class 4 CF
characterised by mutations causing normal CFTR protein production, but w impaired function, resulting in mild or atypical CF symptoms
50
describe class 5 CF
involves mutations that affect CFTR regulation and function, leading to mild or atypical CF symptoms
51
describe class 6 CF
associated w mutations causing reduced CFTR protein stability, resulting in mild or atypical symptoms w residual CFTR function
52
what is the effect of dysfunctional CFTR on the respiratory system
result in production of thick and sticky mucus in airways, making it difficult to clear mucus this leads to chronic airway obstruction, recurrent lung infections, and progressive lung damage
53
what is the effect of dysfunctional CFTR on the digestive system
affects the pancreas, reducing its ability to release enzymes necessary for digestion this leads to malabsorption of nutrients, malnutrition, and GI issues
54
what is the effect of dysfunctional CFTR on the glandular system
leads to salty-tasting skin due to elevated salt levels in sweat, which is a diagnostic feature of CF
55
what is the effect of dysfunctional CFTR on the reproductive system
can cause infertility in both males and females due to issues w production and transport of reproductive fluids
56
describe how genotype can inform management of CF
genotype testing IDs specific mutations in the CFTR gene, allowing healthcare providers to determine the exact genetic profile of an individual w CF it can also guide the selection of mutation-specific medications and therapies allows for tailored and optimal treatment
57
what are 3 management methods for treatment of CF
symptomatic therapy CFTR modulator drugs genetic therapies